Reciprocal feedback regulation between androgen receptor signalling and unfettered signalling through the PI3K-AKT-mTOR pathway in prostate cancer [93, 95] have been shown to inhibit AR signalling and suggest a possible pathway to androgen-independent growth of prostate tumours [93], and conversely, inhibition at each of these signalling nodes was associated with enhanced AR signalling and increased transcription of AR-responsive genes (Figure 1). The gene discussed is AR; the disease is prostate cancer.